DNA repair mechanisms which have been identified in mitotically growing cells of the yeast Saccharomyces cerevisiae are being examined for a) their ability to protect cells undergoing meiosis from DNA-damaging agents, and b) the role of the corresponding genes in normal meiosis. We have developed sucrose gradient techniques to examine repair in mitotic or meiotic cells after low doses of both UV and ionizing radiation and to follow changes in meiotic DNA during meiosis in various rad mutants. Methods have been developed for characterizing rare interruptions in chromosomal DNA as well as locating sites of interruptions in specific chromosomes. There appears to be only one system for excision-repair throughout meiosis; it is controlled by the radl gene product. Cells can tolerate approximately 1500 pyrimidine dimers during early stages of meiosis due to an ability to synthesize DNA past dimers; as cells proceed through meiosis the damage has a greater lethal effect. These results are explained by bypass synthesis that is not associated with molecular recombination; on the contrary, the damage appears to depress recombination at the molecular and genetic levels. The RAD50 and RAD52 genes are essential in the repair of DNA double-strand breaks in mitotic cells. They are also indispensible in normal meiotic development. Mutations in either gene abolish meiotic recombination; however, it appears that RAD50 acts at an earlier step in meiosis. Rare single-strand interruptions (SSIs) were abserved in rad52 strains shorlty after the beginning of meiotic DNA synthesis and these appear to be related to recombination. Gentle isolation techniques have allowed the characterization of SSIs as breaks in DNA rather than gaps. Many of the breaks have 3' OH and 5' PO4 termini. The SSIs do not appear to be randomly distributed based on experiments involving probes for specific chromosomal regions and may correspond to sites or regions involved in normal meiotic recombination.